Hu Zhi-Gao, Zhou Yi, Lin Cheng-Jie, Yuan Guan-Dou, He Song-Qing
Division of Hepatobiliary Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, P.R. China.
Department of General Surgery, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Exp Ther Med. 2021 Mar;21(3):223. doi: 10.3892/etm.2021.9654. Epub 2021 Jan 18.
Hepatic ischemia/reperfusion injury (IRI) is a result of the ischemic cascade and may occur in the settings of liver trauma, resection and transplantation. Components of the complement system have been indicated to be mediators of hepatic IRI and regulators of liver regeneration. As such, their potential to mediate both beneficial and harmful effects render them key targets for therapy. In the present study, the mechanisms of complement mediating hepatic IRI were discussed with a focus on the different functions of complement in hepatic injury and liver recovery, and an explanation for this apparent paradox is provided, i.e. that the complement products C3a and C5a have an important role in liver damage; however, C3a and C5a are also necessary for liver regeneration. Furthermore, situated at the end of the complement activation cascade, the membrane attack complex is crucial in hepatic IRI and inhibiting the complex with a site-targeted murine complement inhibitor, complement receptor 2-CD59, may improve liver regeneration after partial hepatectomy, even when hepatectomy is combined with ischemia and reperfusion.
肝缺血/再灌注损伤（IRI）是缺血级联反应的结果，可能发生于肝外伤、肝切除及肝移植过程中。补体系统的成分已被证实是肝IRI的介质及肝脏再生的调节因子。正因如此，它们介导有益和有害效应的潜能使其成为治疗的关键靶点。在本研究中，我们讨论了补体介导肝IRI的机制，重点关注补体在肝损伤和肝恢复中的不同功能，并对这一明显的矛盾现象做出了解释，即补体产物C3a和C5a在肝损伤中起重要作用；然而，C3a和C5a对肝脏再生也是必需的。此外，位于补体激活级联反应末端的膜攻击复合物在肝IRI中至关重要，用靶向位点的鼠源补体抑制剂补体受体2-CD59抑制该复合物，即使在肝切除联合缺血再灌注的情况下，也可能改善部分肝切除术后的肝脏再生。
